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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prescribing contraceptives to diabetic women requires cognizance of metabolic effects and the risks of type I or type II and gestational diabetes mellitus (GDM) in prediabetic women. Studies have show that poor maternal glycemic control in the 1st trimester in diabetic women has resulted in a twofold to threefold increased risk for congenital malformations. A reduction from 6.6% to 1.1% in malformations could be realized by euglycemic control before conception and during the first 8 weeks of gestation. A low-estrogen preparation should be selected and blood pressure should be monitored regularly. Progestins adversely affect carbohydrate and lipid metabolism, as they decrease glucose tolerance by increased insulin resistance, thus the selection of proper progestin dose/potency is important in prescribing OCs. The lowest-dose OCs may be prescribed under close medical supervision to women with insulin-dependent diabetes mellitus (IDDM) without serious vascular complications. Patients should be evaluated after the 1st cycle of OC use and every 3-4 months thereafter with monitoring of weight, blood pressure, postprandial glucose, and glycosylated hemoglobin levels. Women with prior GDM should be evaluated annually utilizing a 2-hour, 75-g glucose tolerance test (OGTT) at the postpartum visit. For OCs, a low-dose estrogen ( 0.05 mg ethinyl estradiol) and a low-dose/potency progestin (or = 0.50 mg of norethindrone or or= 0.100 mg of levonorgestrel) should be selected. The safety of prescription of OCs to women with type II diabetes is unclear, but a supervised program similar to that of IDDM patients is recommended. Currently neither of the long-term contraceptives, depo-medroxy-progesterone acetate (Depo-Provera) injection or the levonorgestrel-containing implant, Norplant, are recommended as first-time methods for women with diabetes. On the other hand, the IUD is an effective, reversible method, particularly for older women with hypertension, provided antibiotic prophylaxis is undertaken at the time of insertion.
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PMID:Contraception in the diabetic woman. 822 75

Because of their efficacy and ease of use, oral contraceptives (OCs) have become the most widespread contraceptive in France and the world. OCs also have the advantages of reversibility and increasing safety and innocuity due to lower doses of ethinyl estradiol (EE) and improved progestins. The contraceptive effect of OCs depends primarily on suppression of ovulation, endometrial atrophy, and modifications in the cervical mucus rendering it inhospitable to sperm. The three major types of OCs are combined pills of either standard or low dose, sequential pills, and low-dose progestins. Higher dose progestins may also be used for contraception but they are usually reserved for treatment of uterine and mammary pathology. Standard-dose combined OCs contain 50 mcg of EE, while low-dose formulations contain 20-40 mcg. Combined pills are monophasic, biphasic, or triphasic. The advantages of combined OCs are their great efficacy and antigonadotropic power, which allows total steroid doses to be reduced. They may however cause cycle problems due to endometrial atrophy. The long-term administration of EE alone for the first cycle phase with sequential pills has been shown to increase risks of breast disorders, endometrial dysplasia and uterine cancer. Sequential pills are now used only for short-term treatment in specific indications. Low-dose progestins provide a low and continuous dose of progestin. Ovulation is not always inhibited, and persisting secretion of LH and FSH involves some follicular maturation. Contraceptive efficacy relies solely on local effects on the cervical mucus, endometrial atrophy, and decreased tubal motility. The failure rate and incidence of ectopic pregnancy are higher and cycle problems are frequent. The only advantage is the absence of estrogen for women with contraindications. The side effects of combined OCs may include alterations of glucose tolerance and of lipid profiles, increases of blood pressure, modifications in coagulation factors leading to increased thromboembolic risk proportional to the estrogen dose, and increased risk of biliary lithiasis and certain types of jaundice. Combined OCs have not been formally proven to increase risk of cervical cancer, and they are known to have protective effects against ovarian tumors. Most adolescents tolerate standard-dose combined OCs quite well. Low-dose combined pills or high-dose progestins may be appropriate for women over 40. Combined OCs are contraindicated in cases of hypertension, although low-dose progestins may be prescribed. Combined OCs are contraindicated for many diabetics and in all cases of hyperlipidemia and in smokers over 35.
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PMID:[Oral contraception]. 827 87

Oral contraceptives (OCs) were first introduced more than 30 years ago. OC manufacturers have reduced the dosage of synthetic estrogens (e.g., ethinyl estradiol, 100-150 mcg to 20-35 mcg) and progestins to limit their metabolic effects on lipoproteins, carbohydrates, and hemostasis. In addition to protection from pregnancy, OC benefits include lower incidence of painful periods, excessive bleeding, and iron deficiency anemia; reduction of ovarian cysts, benign breast tumors, and pelvic inflammatory disease; and protection against endometrial and ovarian cancers. The risk of a cardiovascular event (myocardial infarction, cerebrovascular events, venous thromboembolism, and deep vein thrombophlebitis) in OC users is 1-2/100,000 women years. Cardiovascular risk factors include smoking, hypertension, lipid disorders, severe obesity, diabetes mellitus, and cardiovascular events in first degree relatives before age 40. Thus, women with any of these risk factors should not use OCs. OCs do not increase the risk of breast cancer in women less than 59 years old. They may increase this risk if used over a long duration before the first fullterm pregnancy. OCs may cause a modest increase in cervical neoplasia. Low-dose OCs have a small effect on lipid metabolism. OCs increase serum triglycerides 30-50%. OCs increase insulin secretion and hyperinsulinemia increases the cardiovascular risk. Practitioners should evaluate clients before prescribing OCs. They should not prescribe OCs to women with hypertension, diabetes mellitus, lipid disorders, gynecological cancers, and previous cardiovascular disorders. Practitioners should tell clients that smoking is a leading risk factor and about OC's side effects (e.g., menstrual disturbances). The physical exam should include a cervical PAP smear, gynecological exam of the uterus and the ovaries, and a breast exam. Practitioners should test cholesterol and triglycerides before and during OC use. Premenopausal healthy women with no risk factors can use low-dose OCs.
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PMID:Update on oral contraception. 836 2

Local or tissue renin angiotensin systems are thought to participate in cardiovascular regulation. However, little information is available on the mechanisms by which renin and angiotensinogen synthesis and secretion are regulated in these tissues. In view of the importance of steroid hormones in the regulation of hepatic angiotensinogen, we have examined the effects of dexamethasone, ethinyl estradiol, or dihydrotestosterone on angiotensinogen gene expression in peripheral or cerebral tissues of Wistar Kyoto (WKY) or spontaneously hypertensive rats (SHR). Following a single injection of dexamethasone (7 mg/kg) the concentrations of angiotensinogen mRNA increased in nearly all organs examined. The differences to controls were higher in SHR than in WKY. Dexamethasone in low doses (10 micrograms/kg/day) given for 10 days did not alter angiotensinogen mRNA or blood pressure in control animals, but increased both parameters in the hypertensive strain. The response to a single dose of ethinyl estradiol (3 mg/kg) was not as uniform as that to dexamethasone, and a tendency for a higher sensitivity was found in SHR. High stimulation rates were found in liver and kidneys of both strains. A single dose of dihydrotestosterone (10 mg/kg) did not significantly affect angiotensinogen mRNA in any organ. Only when a high dose of 50 mg/kg was given daily for 20 days, was angiotensinogen mRNA increased in some tissues. These data indicate that glucocorticoids and estrogens participate in the regulation of angiotensinogen gene expression in several extrahepatic tissues. The higher sensitivity to glucocorticoids in SHR may be relevant for the development of hypertension in this strain.
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PMID:Modulation of tissue angiotensinogen gene expression by glucocorticoids, estrogens, and androgens in SHR and WKY rats. 837 10

It has been demonstrated that high cholesterol levels are correlated with development of atherosclerosis, while high levels of high density lipoprotein (HDL) are associated with reduced cardiovascular mortality. Some endocrine disorders accelerate atherosclerosis in association with hypercholesterolemia, hypertension, low level of HDL and hypertriglyceridemia. In patients with acromegaly, hypertriglyceridemia is sometimes accompanied with and aggravated by the presence of impaired glucose tolerance. In patients with hypothyroidism, coronary atherosclerosis may develop in association with hypertension, hypercholesterolemia and moderate elevation of triglyceride which is often accumulation of intermediate lipoprotein. Cushing syndrome may accelerate atherosclerosis by the fact that corticosteroid may induce or exacerbate several known coronary risk factors including hypertension, hypercholesterolemia and impaired glucose tolerance. Estrogen has beneficial effects on the cardiovascular system for postmenopausal women by affecting lipid metabolism, decrease of LDL and increase of HDL.
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PMID:[Atherosclerosis and endocrine disorders]. 841 91

Widespread application of proven primary and secondary preventive strategies for coronary heart disease would result in substantial savings of life and health care dollars. Proven strategies (excluding lipid therapy) include quitting smoking, treating hypertension, physical activity, aspirin therapy, and appropriate use of anticoagulants, beta blockers, and angiotensin-converting enzyme inhibitors in survivors of myocardial infarction. Estrogen replacement therapy is currently under clinical investigation. Avoidance of obesity and tight control of diabetes are prudent interventions as yet unproved by clinical trials. Unfortunately, preventive strategies are frequently underutilized. The greatest challenge for preventive cardiology is to put into practice what we already know to prevent the development and progression of atherosclerosis.
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PMID:Nonlipid primary and secondary prevention strategies for coronary heart disease. 872 3

The mechanisms of estrogen-induced cardiovascular protection are incompletely understood. Acute estrogen administration enhances acetylcholine-induced vasorelaxation, suggesting that endothelium-dependent factors may be important. The effect of long-term estrogen supplementation on endothelial function has not been well defined. In this double-blind, randomized study, we examined endothelial function in forearm resistance arteries in 11 perimenopausal women before and after 8 weeks of estrogen supplementation (estradiol valerate, 2 mg daily, n = 6) or placebo (n = 5). Forearm blood flow was measured by venous-occlusion plethysmography, and vasoactive agents were infused through a brachial artery cannula in doses that did not influence blood pressure or heart rate. Estrogen supplementation significantly reduced systolic and diastolic pressures but had no effect on plasma lipoproteins. Estrogen did not alter the vasodilator responses to acetylcholine at doses of 9.25, 18.5, and 37 micrograms/min (rise in forearm blood flow before estrogen: 263 +/- 72%, 288 +/- 66%, and 383 +/- 84%, respectively; after estrogen: 205 +/- 34%, 260 +/- 44%, and 359 +/- 54%, P > .05.). Vasodilator responses to the endothelium-independent agent sodium nitroprusside (1.6 micrograms/min) were also unchanged after estrogen supplementation. However, estrogen enhanced vasoconstrictor responses to the nitric oxide synthase inhibitor NG-mono-methyl-L-arginine at doses of 1, 2, and 4 mumol/min (fall in fore-arm blood flow before estrogen: 13 +/- 9%, 20 +/- 7%, and 26 +/- 8%, respectively; after estrogen: 18 +/- 9%, 36 +/- 7%, and 47 +/- 7%, P = .04). Responses to vasoactive agents were unchanged after administration of placebo. Thus, in perimenopausal women, estrogen supplementation reduces blood pressure and enhances basal but not acetylcholine-induced nitric oxide release in fore-arm resistance arteries.
Hypertension 1996 Sep
PMID:Estrogen enhances basal nitric oxide release in the forearm vasculature in perimenopausal women. 918 Jun 41

Cardiovascular disease is the leading cause of death among women, yet clinical trials have not evaluated specific treatment strategies for women. Recently, there has been an expansion of scientific literature exploring differences between women and men with hypertension and cardiovascular disease. The cardioprotective effects of estrogen have been well demonstrated, and the loss of endogenous estrogens with aging contributes to the rapid increase in the incidence of coronary artery disease after menopause. Many of the adverse effects of estrogen deficiency are reversible with estrogen replacement. Estrogen improves lipoprotein profiles, has vasodilatory effects on the endothelium, and inhibits vascular smooth muscle cell growth and constriction. These effects likely all contribute to the reduction in coronary artery disease in the presence of estrogen, and the clinical benefits are not attenuated by concurrent progestins. There are gender-specific differences in the epidemiology of hypertension and coronary artery disease, as well as differences in the pathophysiology and clinical manifestations of disease. Given important experimental interactions between estrogens and the major classes of antihypertensive agents, as well as secondary benefits such as a possible reduction in bone loss with certain agents, a gender-specific approach to hypertension appears to be warranted. Future clinical trials will need to address gender-specific differences in treatment approaches.
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PMID:Gender considerations in hypertension pathophysiology and treatment. 887 71

2-Hydroxylation is one of the major metabolic pathways of estrogens and is believed to be catalyzed by a form of cytochrome P450. Recently it has been reported that estrogen 2-hydroxylase activity in human placenta is catalyzed by aromatase. Some investigators suggested the effect of catechol estrogen on human placental steroidogenesis which may be related to pregnancy-induced hypertension (PIH) through the inhibition of catechol-O-methyltransferase (COMT) activity. In order to better understand the interrelationship between placental aromatase and estrogen 2-hydroxylase activities in PIH patients, both activities were evaluated in the PIH placentas. Human placental microsomes obtained from PIH patients were incubated with [1 beta-3H]androstenedione or [2-3H]estradiol in the presence of NADPH. Aromatase and estrogen 2-hydroxylase activities were assessed by the tritium water method. The immunosuppression patterns of both activities due to monoclonal antiaromatase cytochrome P450 antibody (MAb3-2C2) were studied. Estrogen 2-hydroxylase activity was significantly higher in PIH placentas (4.7 +/- 0.9 pmol/min/mg protein, n = 7) than in normal placentas (3.0 +/- 0.7 pmol/min/mg protein, n = 7). When the PIH placental microsomes were subjected to immunosuppression by 1 to 100 micrograms IgG of MAb3-2C2, estrogen 2-hydroxylase activity was suppressed by 94 to 65% whereas aromatase activity was strongly suppressed by 72 to 17%, respectively. From our results of high estrogen 2-hydroxylase activity in PIH placentas, it is assumed that there is a different estrogen catalyzing mechanism in PIH placentas.
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PMID:Aromatase and estrogen 2-hydroxylase activities of human placental microsomes in pregnancy-induced hypertension. 893 May 23

The aim of this study was to analyze efficacy, tolerance, and adverse events of reversible contraceptives in women with cardiac disease. The authors studied prospectively, during a period of 24-39 (mean = 29) months, 89 women with heart disease of mean age 25.6 (16-42) years. Rheumatic heart disease was present in 73 cases (82%), congenital heart disease in 11 (11%), coronary artery disease in 2 (2%), and cardiomyopathy in 3 (3%). The patients were divided into three groups: GCO--35 patients taking combined oral contraceptives (30 mcg ethinyl estradiol and 75 mg gestodene); GIT--27 patients using injectable progestagens (depot medroxyprogesterone acetate); and GUID--27 patients with IUDs. In the GCO group were found 4 cases (11.4%) of arterial hypertension, 1 (2.8%) of a transient cerebral ischemic attack, 3 (8.5%) of spotting, 1 (2.8%) of amenorrhea, and 1 (2.8%) of pregnancy. Interruption of this method occurred in 4 cases (11.4%): 2 due to hypertension, 1 due to pregnancy, and 1 due to amenorrhea. In the GIT group there were 2 cases (7.4%) of arterial hypertension, 18 (66.6%) of amenorrhea, and 3 (11.1%) of spotting. Interruption of use occurred in 5 cases (18.5%): 2 due to amenorrhea, 2 due to weight gain, and 1 due to headache. In the GUID group there was 1 case (3.7%) of infection, 1 (3.7%) of pregnancy, and 1 (3.7%) of spontaneous expulsion of the IUD. Interruption of use took place in 3 cases (11.1%): 1 due to infection, 1 due to pregnancy, and 1 due to expulsion. The comparison between the groups demonstrated a difference in the incidence of amenorrhea (p 0.005) and method discontinuation (p 0.025). Use of reversible contraceptives in women with heart disease was associated with an acceptable cardiovascular risk. Efficacy and side effects of the methods were comparable in the groups; however, intolerance was observed more in the GIT group. (author's modified)
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PMID:[Contraceptive use in women with heart disease]. 893 85


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